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  4. Mathematical model of heterogeneous cancer growth with an autocrine signalling pathway
 
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Mathematical model of heterogeneous cancer growth with an autocrine signalling pathway

Journal
Cell Proliferation
Journal Volume
45
Journal Issue
5
Pages
445-455
Date Issued
2012
Author(s)
Hu, G.-M.
Lee, C.-Y.
Chen, Y.-Y.
NING-NING PANG  
Tzeng, W.J.
DOI
10.1111/j.1365-2184.2012.00835.x
URI
http://www.scopus.com/inward/record.url?eid=2-s2.0-84865563252&partnerID=MN8TOARS
http://scholars.lib.ntu.edu.tw/handle/123456789/371244
Abstract
Objectives: Cancer is a complex biological occurrence which is difficult to describe clearly and explain its growth development. As such, novel concepts, such as of heterogeneity and signalling pathways, grow exponentially and many mathematical models accommodating the latest knowledge have been proposed. Here, we present a simple mathematical model that exhibits many characteristics of experimental data, using prostate carcinoma cell spheroids under treatment. Materials and methods: We have modelled cancer as a two-subpopulation system, with one subpopulation representing a cancer stem cell state, and the other a normal cancer cell state. As a first approximation, these follow a logistical growth model with self and competing capacities, but they can transform into each other by using an autocrine signalling pathway. Results and conclusion: By analysing regulation behaviour of each of the system parameters, we show that the model exhibits many characteristics of actual cancer growth curves. Features reproduced in this model include delayed phase of evolving cancer under 17AAG treatment, and bi-stable behaviour under treatment by irradiation. In addition, our interpretation of the system parameters corresponds well with known facts involving 17AAG treatment. This model may thus provide insight into some of the mechanisms behind cancer. ? 2012 Blackwell Publishing Ltd.
SDGs

[SDGs]SDG3

Other Subjects
tanespimycin; article; cancer growth; cancer radiotherapy; cancer research; cancer therapy; mathematical model; prostate carcinoma; Autocrine Communication; Benzoquinones; Cell Proliferation; HSP90 Heat-Shock Proteins; Humans; Lactams, Macrocyclic; Logistic Models; Neoplasms; Phenotype; Radiation Dosage; Signal Transduction
Type
journal article

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